Search

A conscious shaping of entrepreneurial competence is a relevant element of entrepreneurial education. In order to recognize which of the competencies regarded as entrepreneurial are characteristic of members of entrepreneurial teams, which is crucial for the work of those teams, it is necessary to identify the structure of those competencies. This quantitative study was conducted with the use of a survey method and involved 111 entrepreneurs working within 48 entrepreneurial teams. The main objective of the research was to verify the compliance of entrepreneurial competence with the effectual vs. causal approach, which would allow us to answer the question regarding which of these approaches characterizes entrepreneurs to a greater extent. This study aimed to examine which entrepreneurial competencies characterize entrepreneurs working in entrepreneurial teams, to verify them with the effectual vs. causal approach, and to define their internal structure. The results of this research revealed that the competencies related to the effectual approach are indicated to more frequently and strongly characterize the surveyed entrepreneurs. Additionally, an exploratory factor analysis enabled the identification of three main, internally consistent groups of elements forming the competence structure of the surveyed entrepreneurs. Our results may be used in the development and modernization of curricula and courses in entrepreneurship education.

In the situation of a permanent change and increased competition, business ventures are more and more often undertaken not by individuals but by entrepreneurial teams. The main aim of this paper is to examine the team principles implemented by effective entrepreneurial teams and how they differ in nascent and established teams. We also focused on the relationship between the implementation of these rules by entrepreneurial team members and their evaluation of venture performance and personal satisfaction. The quantitative method was used: a list of nine items describing the principles important for the entrepreneurial teams' collaboration was included in a questionnaire conducted in a group of 106 Polish entrepreneurs who run their businesses as members of entrepreneurial teams. The results of the research showed that all the collaboration principles included in the prepared scale are implemented by the tested entrepreneurial teams; in the case of two particular items, the obtained scores were higher in nascent teams. The correlation between principle implementation and venture performance as well as the correlation between principle implementation and entrepreneurs' professional satisfaction was confirmed. In addition, the goal was to emphasize the importance of the entrepreneurial team's collaboration due to its effectiveness, and propose the prepared scale as a tool for entrepreneurial reflective learning. Finally, statements by members of two entrepreneurial teams concerning team collaboration are presented to deliver case studies that can be used during entrepreneurship courses.

Variation in ATG16L1, a protein involved in autophagy, confers risk for Crohn's disease, but mice with hypomorphic ATG16L1 activity do not develop spontaneous intestinal inflammation; this study shows that autophagy compensates for endoplasmic reticulum stress -- common in inflammatory bowel disease epithelium -- specifically in Paneth cells, with Crohn's-disease-like inflammation of the ileum originating from this cell type when both pathways are compromised. Inflammation in Crohn's disease Variations in ATG16L1 -- a protein involved in autophagy -- are risk factors for Crohn's disease, but although mice homozygous for a common ATG16L1 risk allele show abnormal Paneth cell function, they do not develop intestinal inflammation as might be expected. Richard Blumberg and colleagues show that impairment of either autophagy or the unfolded protein response within Paneth cells results in each other's compensatory engagement, but that colitis develops only when both pathways are impaired. This work highlights pharmacological augmentation of autophagy as a possible therapeutic approach to controlling intestinal inflammation. The recognition of autophagy related 16-like 1 (ATG16L1) as a genetic risk factor has exposed the critical role of autophagy in Crohn's disease.sup.1. Homozygosity for the highly prevalent ATG16L1 risk allele, or murine hypomorphic (HM) activity, causes Paneth cell dysfunction.sup.2,3. As Atg16l1.sup.HM mice do not develop spontaneous intestinal inflammation, the mechanism(s) by which ATG16L1 contributes to disease remains obscure. Deletion of the unfolded protein response (UPR) transcription factor X-box binding protein-1 (Xbp1) in intestinal epithelial cells, the human orthologue of which harbours rare inflammatory bowel disease risk variants, results in endoplasmic reticulum (ER) stress, Paneth cell impairment and spontaneous enteritis.sup.4. Unresolved ER stress is a common feature of inflammatory bowel disease epithelium.sup.4,5, and several genetic risk factors of Crohn's disease affect Paneth cells.sup.2,4,6,7,8,9. Here we show that impairment in either UPR (Xbp1.sup.[DELTA]IEC) or autophagy function (Atg16l1.sup.[DELTA]IEC or Atg7.sup.[DELTA]IEC) in intestinal epithelial cells results in each other's compensatory engagement, and severe spontaneous Crohn's-disease-like transmural ileitis if both mechanisms are compromised. Xbp1.sup.[DELTA]IEC mice show autophagosome formation in hypomorphic Paneth cells, which is linked to ER stress via protein kinase RNA-like endoplasmic reticulum kinase (PERK), elongation initiation factor 2[alpha] (eIF2[alpha]) and activating transcription factor 4 (ATF4). Ileitis is dependent on commensal microbiota and derives from increased intestinal epithelial cell death, inositol requiring enzyme 1[alpha] (IRE1[alpha])-regulated NF-[kappa]B activation and tumour-necrosis factor signalling, which are synergistically increased when autophagy is deficient. ATG16L1 restrains IRE1[alpha] activity, and augmentation of autophagy in intestinal epithelial cells ameliorates ER stress-induced intestinal inflammation and eases NF-[kappa]B overactivation and intestinal epithelial cell death. ER stress, autophagy induction and spontaneous ileitis emerge from Paneth-cell-specific deletion of Xbp1. Genetically and environmentally controlled UPR function within Paneth cells may therefore set the threshold for the development of intestinal inflammation upon hypomorphic ATG16L1 function and implicate ileal Crohn's disease as a specific disorder of Paneth cells., Author(s): Timon E. Adolph [sup.1] , Michal F. Tomczak [sup.2] , Lukas Niederreiter [sup.1] , Hyun-Jeong Ko [sup.2] [sup.17] , Janne Böck [sup.3] , Eduardo Martinez-Naves [sup.4] , Jonathan N. [...]